Nicotinic acid induces apolipoprotein A-I gene expression in HepG2 and Caco-2 cell lines

Haas, Michael J.; Alamir, Abdul-Razzak; Sultan, Senan; Chehade, Joe; Wong, Norman C.; Mooradian, Arshag D.

doi:10.1016/j.metabol.2011.05.005

Cited by 13 publications

(9 citation statements)

References 26 publications

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“…The primer sequences for quantitative RT-PCR of OPN and Apo-A1 were obtained from the previous reports [Hahnel et al, 2010;Haas et al, 2011]. Then, quantitative RT-PCR was performed with SYBR Green PCR Master Mix (Applied Biosystems) using CFX96 realtime PCR system (Bio-Rad).…”

Section: Quantitative Rt-pcr Of Opn and Apo-a1mentioning

confidence: 99%

Suppressive effect of the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) on hepatitis C virus replication

Sato

Saito

Sugiyama

et al. 2013

J of Cellular Biochemistry

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The histone deacetylase (HDAC) inhibitor suberoylanilide hydroxamic acid (SAHA) has a clinical promise for treatment of cancer including hepatocellular carcinoma (HCC). To investigate effect of SAHA on hepatitis C virus (HCV) replication, we treated the HCV replicon cell OR6 with SAHA. HCV replication was significantly inhibited by SAHA at concentrations below 1 μM with no cellular toxicity. Another HDAC inhibitor, tricostatin A, also showed reduction of HCV replication. The microarray analysis and quantitative RT-PCR demonstrated up-regulation of osteopontin (OPN) and down-regulation of apolipoprotein-A1 (Apo-A1) after SAHA treatment. Direct gene induction of OPN and knockdown of Apo-A1 also showed reduction of HCV replication. The liver specific microRNA-122, which is involved in HCV replication, was not affected by SAHA treatment. These results suggest that SAHA has suppressive effect on HCV replication through alterations of gene expression such as OPN and Apo-A1 in host cells. Epigenetic treatment with HDAC inhibitors may be a novel therapeutic approach for diseases associated with HCV infection such as chronic hepatitis, liver cirrhosis, and HCC.

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Section: Quantitative Rt-pcr Of Opn and Apo-a1mentioning

confidence: 99%

Suppressive effect of the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) on hepatitis C virus replication

Sato

Saito

Sugiyama

et al. 2013

J of Cellular Biochemistry

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“…Niacin acts at many sites in lipoprotein metabolism. Niacin may decrease hepatic TG-rich lipoprotein secretion by decreasing post-prandial free fatty acid levels and by decreasing hepatic diacylglycerol transferase (DGAT) levels [66,67,68]. Niacin, in combination with colestipol [14] or alone [69] decreased sdLDL levels and increased HDL 2 levels.…”

Section: Drug Effects On Hl and Hdl And Ldl Particlesmentioning

confidence: 99%

“…The changes in sdLDL and HDL 2 are mediated by changes in HL activity. Finally, niacin increased HDL cholesterol by increasing apoAI secretion [67,68] and by impairing HDL catabolism [70], presumably, by decreasing HL activity.…”

Section: Drug Effects On Hl and Hdl And Ldl Particlesmentioning

confidence: 99%

The effect of hepatic lipase on coronary artery disease in humans is influenced by the underlying lipoprotein phenotype

Brunzell

Zambón

Deeb

2012

Biochimica et Biophysica Acta (BBA) - Molecular and Cell Biolog

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Increased or decreased hepatic lipase (HL) activity has been associated with coronary artery disease (CAD). This is consistent with the findings that gene variants that influence HL activity were associated with increased CAD risk in some population studies but not in others. In this review, we will explain the conditions that influence the effects of HL on CAD. Increased HL is associated with smaller and denser LDL (sdLDL) and HDL (HDL3) particles, while decreased HL is associated with larger and more buoyant LDL and HDL particles. The effect of HL activity on CAD risk is dependent on the underlying lipoprotein phenotype or disorder. Central obesity with hypertriglyceridemia (HTG) is associated with high HL activity that leads to the formation of sdLDL that is proatherogenic. In the absence of HTG, where large buoyant cholesteryl ester-enriched LDL is prominent, elevation of HL does not raise the risk for CAD. In HTG patients, drug therapy that decreases HL activity selectively decreases sdLDL particles, an antiatherogenic effect. Drug therapy that raises HDL2 cholesterol has not decreased the risk for CAD. In trials where inhibition of cholesterol ester transfer protein (CETP) or HL occurs, the increase in HDL2 most likely is due to inhibition of catabolism of HDL2 and impairment of reverse cholesterol transport (RCT). In patients with isolated hypercholesterolemia, but with normal triglyceride levels and big-buoyant LDL particles, an increase in HL activity is beneficial; possibly because it increases RCT. Drugs that lower HL activity might decrease the risk for CAD only in hypertriglyceridemic patients with sdLDL by selectively clearing sdLDL particles from plasma, which would override the potentially pro-atherogenic effect on RCT.

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“…Another potent part of their study was the determination of molecular mechanism of the effects of nicotinic acid via its responsive element on apo A-I promoter. [19] We measured the apo A-I mRNA levels after treatment with UII in time-dependent experiments, but there were not significant changes between treated cells compared with control cells (Data not shown).…”

Section: Discussionmentioning

confidence: 97%

“…[4] Apolipoprotein A-I, as the major protein on HDL surface, is a ligand for adenosine triphosphate-binding cassette (ABC) transporters which mediate efflux of cholesterol from cells to HDL particles. [19]…”

Section: Discussionmentioning

confidence: 99%

Effect of urotensin II on apolipoprotein B ₁₀₀ and apolipoprotein A-I expression in HepG2 cell line

2014

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Background:Increased apolipoprotein B100 (apo B) and decreased apolipoprotein A-I (apo A-I) production are important risk factors in atherosclerosis. Urotensin II (UII), as the most potent vasoconstrictor in human, is related with hypertension and probably atherosclerosis. Because of the relationship between the hypertension and lipoprotein metabolism in atherosclerosis, the aim of this study was to test the effect of urotensin II on apo B and apo A-I expression in hepatic (HepG2) cell line.Materials and Methods:HepG2 cells were treated with 10, 50, 100, and 200 nmol/L of urotensin II (n = 6). Relative apo B and apo A-I messenger RNA (mRNA) levels in conditioned media, normalized to glyceraldehyde-3-phosphate dehydrogenase, were measured with quantitative real-time polymerase chain reaction method. In addition, apo B and apo A-I levels were also estimated and compared with the controls using the western blotting method. Data were analyzed statistically by ANOVA and non-parametric tests.Results:The apo B mRNA levels were not increased significantly following the treatment with UII. However, apo B protein levels were increased significantly after the treatment with urotensin II, especially at 100 and 200 nmol/L. The apo A-I mRNA and protein levels in conditioned media also were not significantly changed. However, there was a significant decrease in apo A-I mRNA and protein levels at 200 nM UII.Conclusions:UII might increase apo B at protein level probably through participating factors in its synthesis and/ or stability/degradation. In addition, UII may have decreasing effect at more than 200 nM concentrations on apo A-I.

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Nicotinic acid induces apolipoprotein A-I gene expression in HepG2 and Caco-2 cell lines

Cited by 13 publications

References 26 publications

Suppressive effect of the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) on hepatitis C virus replication

Suppressive effect of the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) on hepatitis C virus replication

The effect of hepatic lipase on coronary artery disease in humans is influenced by the underlying lipoprotein phenotype

Effect of urotensin II on apolipoprotein B ₁₀₀ and apolipoprotein A-I expression in HepG2 cell line

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Nicotinic acid induces apolipoprotein A-I gene expression in HepG2 and Caco-2 cell lines

Cited by 13 publications

References 26 publications

Suppressive effect of the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) on hepatitis C virus replication

Suppressive effect of the histone deacetylase inhibitor suberoylanilide hydroxamic acid (SAHA) on hepatitis C virus replication

The effect of hepatic lipase on coronary artery disease in humans is influenced by the underlying lipoprotein phenotype

Effect of urotensin II on apolipoprotein B 100 and apolipoprotein A-I expression in HepG2 cell line

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Effect of urotensin II on apolipoprotein B ₁₀₀ and apolipoprotein A-I expression in HepG2 cell line